Many individual studies have reported that patients with essential hypertension have: a) increased plasma levels of norepinephrine while young, b) a decreased response to infusions of the beta-adrenergic agonist isoproterenol, c) abnormal binding to leukocyte beta-adrenergic receptors and, d) decreased clearance of plasma 3-H-norepinephrine. We have found that beta-blocking drugs slow catecholamine clearance and beta-agonists increase catecholamine clearance and desensitize beta-receptors. The above observations suggest that abnormal catecholamine clearance, increased catecholamine levels, and decreased beta-receptor sensitivity in hypertensives are related. For example, diminished catecholamine uptake could lead to high catecholamine levels and desensitized beta-receptors. We propose to study all these defects in the same hypertensive subjects to determine if these abnormalities are linked. Hypertensives and controls will have catecholamine uptake-1 and uptake-2 clearance rates quantitated. Norepinephrine release rate will be calculated, and in vivo and in vitro beta-receptor sensitivity measured. Hypertensives and normal subjects will then be given propranolol, which slows uptake-2, and have their catecholamine levels and clearance rate measured. Hypertensive patients will have their endogenous catecholamine release pharmacologically decreased to see if beta-receptor sensitivity returns to normal and to measure the effect on catecholamine clearance. This study of several of the better documented adrenergic abnormalities in hypertensive patients will determine if the individual defects correlate with each other. It will be a first step to see if these defects can be linked to one another and to the pathogenesis of hypertension.